Transcription factor Stat3 stimulates metastatic behavior of human prostate cancer cells in vivo, whereas Stat5b has a preferential role in the promotion of prostate cancer cell viability and tumor growth.

Transcription factor Stat3 stimulates metastatic behavior of human prostate cancer cells in vivo, whereas Stat5b has a preferential role in the promotion of prostate cancer cell viability and tumor growth.

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http://www.wikidata.org/entity/Q33745272

Q33745272

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STAT3 protein up-regulates Gα-interacting vesicle-associated protein (GIV)/Girdin expression, and GIV enhances STAT3 activation in a positive feedback loop during wound healing and tumor invasion/metastasis The tumor suppressor hTid1 inhibits STAT5b activity via functional interaction Procyanidin B2 3,3(″)-di-O-gallate, a biologically active constituent of grape seed extract, induces apoptosis in human prostate cancer cells via targeting NF-κB, Stat3, and AP1 transcription factors.Elevated YKL40 is associated with advanced prostate cancer (PCa) and positively regulates invasion and migration of PCa cells Unexploited therapies in breast and prostate cancer: blockade of the prolactin receptor.Pharmacologic inhibition of Jak2-Stat5 signaling By Jak2 inhibitor AZD1480 potently suppresses growth of both primary and castrate-resistant prostate cancer.Inhibition of STAT3 signaling targets both tumor-initiating and differentiated cell populations in prostate cancer.Reconstruction and analysis of transcription factor-miRNA co-regulatory feed-forward loops in human cancers using filter-wrapper feature selection.Protein-network modeling of prostate cancer gene signatures reveals essential pathways in disease recurrence.Signal transducer and activator of transcription 5a/b: biomarker and therapeutic target in prostate and breast cancer Structure-Based Screen Identifies a Potent Small Molecule Inhibitor of Stat5a/b with Therapeutic Potential for Prostate Cancer and Chronic Myeloid Leukemia.STAT5A-mediated SOCS2 expression regulates Jak2 and STAT3 activity following c-Src inhibition in head and neck squamous carcinoma Inhibition of Stat5a/b Enhances Proteasomal Degradation of Androgen Receptor Liganded by Antiandrogens in Prostate Cancer.Targeting the insulin growth factor and the vascular endothelial growth factor pathways in ovarian cancer.Jak2-Stat5a/b Signaling Induces Epithelial-to-Mesenchymal Transition and Stem-Like Cell Properties in Prostate Cancer Genome scan study of prostate cancer in Arabs: identification of three genomic regions with multiple prostate cancer susceptibility loci in Tunisians.STAT5A/B gene locus undergoes amplification during human prostate cancer progression.Critical role of the WASF3 gene in JAK2/STAT3 regulation of cancer cell motility.Prostate cancer: the need for biomarkers and new therapeutic targets.Androgen receptor-dependent and -independent mechanisms driving prostate cancer progression: Opportunities for therapeutic targeting from multiple angles.Targeting transcription factor Stat5a/b as a therapeutic strategy for prostate cancer.Prolactin regulation of the prostate gland: a female player in a male game.Dissecting Major Signaling Pathways throughout the Development of Prostate Cancer.The role of transcription factors in prostate cancer and potential for future RNA interference therapy.The involvement of JAK-STAT3 in cell motility, invasion, and metastasis.STAT3 in Cancer-Friend or Foe?Robust gene network analysis reveals alteration of the STAT5a network as a hallmark of prostate cancer.Prolactin- and testosterone-induced carboxypeptidase-D correlates with increased nitrotyrosines and Ki67 in prostate cancer.A STAT inhibitor patent review: progress since 2011.Pharmacological methyl group donors block skeletal metastasis in vitro and in vivo.Growth hormone enhances LNCaP prostate cancer cell motility.Pharmacologic suppression of JAK1/2 by JAK1/2 inhibitor AZD1480 potently inhibits IL-6-induced experimental prostate cancer metastases formation.IL-23 selectively promotes the metastasis of colorectal carcinoma cells with impaired Socs3 expression via the STAT5 pathway.Nuclear Stat5a/b predicts early recurrence and prostate cancer-specific death in patients treated by radical prostatectomy.Inhibition of Stat3 activation by sanguinarine suppresses prostate cancer cell growth and invasion N-terminal truncation of Stat5a/b circumvents PIAS3-mediated transcriptional inhibition of Stat5 in prostate cancer cells.Cancer Chemopreventive Potential of Procyanidin STAT3 and STAT5A are potential therapeutic targets in castration-resistant prostate cancer.STAT5A/B Blockade Sensitizes Prostate Cancer to Radiation through Inhibition of RAD51 and DNA Repair.17β-Estradiol and ICI182,780 Differentially Regulate STAT5 Isoforms in Female Mammary Epithelium, With Distinct Outcomes.

P2860

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P2860

Transcription factor Stat3 stimulates metastatic behavior of human prostate cancer cells in vivo, whereas Stat5b has a preferential role in the promotion of prostate cancer cell viability and tumor growth.

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http://www.wikidata.org/entity/Q33745272

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2010 nî lūn-bûn

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2010 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2010 թվականի փետրվարին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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